Fig. 1

Generating Abl∆IDR and testing its ability to rescue adult and embryonic viability. a Diagram of human Abl and Arg and Drosophila Abl, showing conserved domains/motifs as well as motifs in the IDR that vary between family members. b All Abl family members share a region between the structured kinase and F-actin binding domains that is predicted to be disordered. Graphical report of unstructured regions from the D²P² database for human Abl and Arg and Drosphila Abl. Nine different disorder predictions (depicted by the pastel-colored blocks) are stacked and aligned with the amino sequence for each protein (depicted in black) and the structured domains (depicted with colored blocks) within the polypeptide chain. c Illustration of the mutant Abl proteins we previously tested and our new Abl∆IDR mutant. It was designed to remove essentially the entire IDR, leaving only a few amino acids at each end to ensure we did not disrupt folding of the kinase domain or FABD. A 15 amino acid flexible linker was added in its place. d Assessment of the ability of Abl∆IDR to rescue the viability of abl⁴/DfAbl adults, normalized to rescue by our wildtype Abl transgene, and compared to rescue by some of our previously tested mutants. Line indicates degree of rescue relative to wildtype Abl transgene. Full data sets with statistical significance for D-F are in Table 1. e Assessment of the ability of Abl∆IDR to rescue embryonic viability of the progeny of abl⁴/DfAbl females mated to abl⁴/+ males, compared to rescue by some of our previously tested mutants. Line indicates 100% embryonic viability. f Assessment of the ability of Abl∆IDR to rescue embryonic viability of the progeny females with germlines homozygous for of abl⁴ mated to abl⁴/+ males, compared to rescue by some of our previously tested mutants. Line indicates degree of rescue by our wildtype Abl transgene